Review 2

The Truth About Stuff You Eat.

Review 2 - Published December 2007

Monte WC. 2007, A Deadly Experiment – (Fitness Life 2007 Dec.34:38-42)


We cannot introduce a poison into the food supply without paying a terrible price, and I am convinced that this tragic scenario has and is playing itself out. In an earlier article regarding the dangers of Aspartame (Fitness Life 2007 Nov 33:31-33), I explained how this artificial sweetener can degrade into methanol and then into formaldehyde, and I touched on some of the deleterious effects of formaldehyde on the human body. In this article I make the case that increased methanol consumption is implicated in the appearance and increased incidence of multiple sclerosis (MS) and that Aspartame consumption is one of the two primary sources of methanol in our diets.


What Price Aspartame: The Early Warnings Ignored


We have consumption data for Aspartame in the United States from mid-1981 when a ban on its use was reversed through political intervention (39). The increase in production and consumption was relatively slow until a surge occurred when approval came for its use in carbonated beverages. Although we would wish such periods did not occur, a period in which a substance is introduced into the diet of an unsuspecting population is a perfect time to look for anomalies that can help us to hypothesize about the extent to which the substance may be toxic. I examined data on diseases and conditions that I thought might be affected by the increased consumption of Aspartame such as depression, autoimmunity, and birth defects (terata). Both methanol and Aspartame are proven teratogens in animals far less sensitive to methanol than humans (92,96,103-105,124,159,177). Data from the US National Center for Health Statistics regarding morbidity numbers during those critical early years are presented here in graphic form.


These are the original data with no modification save for those regarding autism; these were displaced by six years because the data presented to me were for patients diagnosed at six years of age(98). This displacement reflects that exposure to methanol occurred in the womb.


If these data teach us anything they teach us that the first question we should ask a depressed child is “Do you drink diet soda?”…and that pregnancy is not the time to consume Aspartame(100).


It is interesting to note that Breast Cancer has the same worldwide distribution and incidence characteristics as MS (190) and shares with MS the known, methanol rich, causal agentÂ…cigarette smoking.


I found the most striking graph to be the one showing increase in diagnosed cases of multiple sclerosis. It usually takes, at least, 10 years from first onset of symptoms to reportable diagnosis of the disease(86,167). This early reporting was evidence, to me, of much worse to follow.


Science has been seeking the cause of multiple sclerosis for 150 years. It has repeatedly been suggested there is evidence to implicate a small toxic molecule(153,185)Â… a solvent(74,140). Methanol is the smallest of solvents.


The results of 27 years of Aspartame consumption


The Worst of Timing

The 1980’s was well into the era when laboratories that had been performing methanol toxicity research were being paid by the company who invented Aspartame to prove the safety of its sweetener(121,131). Dr. Hugo Henzi, an M.D. now deceased, published a book in 1980 purporting to prove dietary methanol as the cause of multiple sclerosis(5). His clinical logic and anatomical observations were impeccable (6,8-10), but he made a major mistake. He erroneously believed that the methanol that caused MS came from “fresh” fruits and vegetables, and as a consequence, he proposed a curative diet that we now know had little chance of success(101). However, several lines of evidence are now converging to support Dr. Henzi’s primary assertion.


The Secret Battle that is Autoimmunity

From an early moment in the evolution of manÂ…from as far back as the mutation that accounted for universality in its distributionÂ… a biochemical battle has quietly raged within the most intimate anatomy of the human body. Two alcohols competing for the attention of a serendipitously distributed and poorly understood enzymeÂ… an enzyme that, by accident, has become the lonely suitor to and only benefactor of their advances. The outcome, after years of struggle, determines who will and who will not die with MS.


The alcohols are ethyl and methyl alcohol. Methanol is the smallest known alcohol containing only one carbon atom; ethanol has two carbon atoms. The enzyme has had several names as it has been discovered and rediscovered over the years in the physiological, neurological, and opthomological sciences. However, it is most commonly referred to as ADH (alcohol dehydrogenase). ADH is known to serve a number of functions in the healthy human body. In the retina it is called retinal reductase and plays a major role in vision (112), but ADH’s ability to convert alcohols to aldehydes is what is paramount to our discussion here. ADH is a large protein molecule and due to its unique structure it much “prefers” coupling with ethanol, which it converts to acetaldehyde that our body uses for many good purposes. It is only when ADH finds no ethanol in the blood or when the methanol concentration in the blood is 10 times greater than that for ethanol that ADH slowly and “reluctantly” turns methanol into formaldehyde(113,114,116-118,122). Only a small amount of ethanol in one’s blood prevents methanol from turning into formaldehyde (141). This is fortunate for without this inhibiting effect on formaldehyde formation humans would have become extinct eons ago.


Another bit of good fortune for the majority of those in the human race is something that was noticed during the development of breath analyzers for the detection of drunk drivers and subsequently confirmed in the scientific literature. That is, we nearly always have ethanol, circulating in our bloodstreams (64,188). The presence of ethanol is the natural outcome of digesting plant material in the gut(134,174), but the amounts of this endogenous ethanol in our blood varies greatly across individuals(64,173). No ethanol could be found in the blood of some subjects while others have high enough ethanol in their blood to be considered impaired (186). Individual differences in the presence of endogenous ethanol (and the location of tissue containing ADH) may well account for why some people die or become blind from a teaspoon of methanol(16) and some consume it, mixed with ethanol, as a preferred source of intoxication(110). I also believe that these individual differences in the presence of endogenous ethanol provides an explanation for why some people develop autoimmune disease and others do not, no matter what they consume or smoke.


Interestingly the location of ADH in our bodily tissue seems to vary with our genetic makeup(187). ADH might, for reasons not fully understood, be found in the liver, gut, brain, eye, skin and sinew. These hereditary differences are most likely responsible for the varied manifestations of autoimmunity. Higher enzyme representation in the brain might predispose the individual to develop MS while its presence in the skin would be required for the evolution of lupus.


Autoimmunity: Teaching our Body to Produce Antibodies against our own tissue.

During the evolution of vaccines, not long after the pioneering work of Jennings and Pasture, the pharmaceutical industry noticed and took good advantage of the “trick” of toxoid production(75,114,179). A toxoid is a bacterial or viral protein that has been treated in the laboratory with a low concentration of formaldehyde (26). The concentration is just enough to attract the attention of the macrophage but not enough to completely change the protein’s structure. The toxoid (vaccine) is injected into humans who then produce antibodies and thus develop immunity to the original, offending organism. It is interesting to note that injection of the original protein without formaldehyde treatment often causes little or no antibody production and therefore little immunity to that bacterium or virus.

As discussed in my previous article, once methanol is changed into formaldehyde and then, by water, to formal hydrate (4,27,114), all hell breaks lose.

Unbeknownst to most researchers, formal hydrate is extremely acidic(114) along with being a powerful esterifying agent (122). These two characteristics make it irresistibly attractive to our bodyÂ’s protein molecules, especially to those found in the insulation of the human brain(18,53). Opposites attract and the basic protein (MBP) of myelin quickly falls prey to acidic formal hydrate.

Macrophages are large white, amoeba like blood cells for which the major purpose in our body is to destroy attacking life forms and consume foreign and broken protein from our bodies. For reasons yet unknown, evolution has equipped macrophages with chemical receptors to detect and destroy specifically and with great vigor protein treated with formaldehyde (23,24,25). Macrophages can signal the immune system to produce antibodies to the proteins that they consume. This is a dark side to the good work of the macrophage. What happens when the protein in our brain comes in contact with formaldehyde from diet soda?


An Increase in MS

There is no denying…there has been an epidemic of autoimmune disease throughout the world over the last 30 years (79,79a-j,80,80a-c,81,81a,82). Multiple sclerosis, once almost unknown in Japan( 44,85,168), has now risen to menace a large portion of the population(81,81a). The lower latitudes and warmer climates once “mysteriously” protected from the full brunt of this tragically debilitating disease (83,85,168) have seen incidence and prevalence of MS climb to as much as four times what they were in the days before summer drinks were sweetened with Aspartame (79,79b,79d,79f,g,h,79j,80,80a-c). The United States which has long had a relatively high MS incidence has seen at least a 50% increase (77). Medical journals in Australia (82) and New Zealand (90) both report unexplainable increases in their inordinately high(168) “infection” rates.



Where Does Methanol Come from Aside from Aspartame?


Cigarette Smoking

After 150 years of study of MS only cigarette smoking is universally accepted as a causative agent(67-70,70a-d,71). Smoking has also been causally linked to the progression of MS, transforming a relapsing-remitting clinical course into a much more serious secondary progressive course (69). Tobacco leaves contain large amounts of pectin; and although most scientists are unaware of this, tobacco leaves are left in barns to ferment for weeks (61,62,66). This fermentation releases much of the available methanol from the pectin into the moisture content of the tobacco before it is sold to be made into cigarettes (65). Consequently, methanol is one of the most abundant toxic compounds found in cigarette smoke (63). Methanol is found in human breath following smoking (64) indicating a presence in the blood. A large case-controlled study, mostly of prevalent disease, has shown that systemic lupus erythematosus (SLE) is also positively associated with cigarette smoking and inversely associated with alcohol consumption(73).


Food Processing

Although acknowledging the role played by smoking, I believe that food processing and preserving is what first dramatically increased methanol consumption. At some point in our genetic history a mutation occurred that disrupted the ability of liver catalase enzyme’s to quickly and safely clean methanol from our blood (52). For several million years after this mutation there was no downside to the mutation, no autoimmunity. We ate fresh food, and what very little methanol is in fresh fruits and vegetables is countered by their own ethanol content (1,28,29)and their ubiquitous gift for slow, steady ethanol production in the gut(64,134,188). However, when the fruits and vegetables and their naturally occurring pectin is placed in a sealed container (as in canning) that is then sterilized, heated or even just stored at room temperature for months, the normally unavailable, chemically bound methanol is released from the pectin (1,28,29,34). The methanol slowly builds up, trapped in the container, to hundreds of times more than when fresh(28,29). Very simply it is “canned” fruits and vegetables that were (before aspartame) the major source of free methanol in the human diet.



The History of MS Recapitulates the History of the Canning Industry

Nicolas Appert invented canning in the 1790s, and the first canning factory was fully operational in England by 1813 (46). Due to the expense, early canning was undertaken primarily with meats which have no pectin content and therefore would not have caused methanol accumulation. However, canning of fruits and vegetables followed. Over time canning became more prevalent and less expensive(46), and the consumption of canned food skyrocketed as did the incidence of multiple sclerosis. As the canning industry flourished so did the practice of incorporating into recipes the “natural”, methanol-laden juices from canned fruits and vegetables rather than throwing them away(74).


The first documented case of multiple sclerosis was reported by Jean-Martin Charcot in a lecture in 1868(45), although it is thought that the “first identifiable instance of MS” was that of Augustus d”Este whose symptoms started between 1822 and 1843(45). During the 19th century MS was recognized as a disease but considered “quite rare” with Charcot reporting fewer than 40 cases during his long career(45). Increasing numbers of cases were reported in the late 19th century(45). Although co-occurrence is not proof of causality, similarities in initial appearance and in rate of increasing incidence are consistent with a close linkage between MS and consumption of canned fruits and vegetables.



Explaining the Unexplainable


MS a Disease of the Colder Countries

The differential prevalence of MS across different geographical regions also supports this linkage. The “latitude gradient theory” of MS is a way to explain the occurrence of higher MS prevalence in colder regions of the world (168). The tropics have until recently been blessed with very low incidence of MS (83,85,168). These warmer climes are, of course, regions in which the on-going supply of fresh fruits and vegetables has obviated the need for more expensive, canned produce, hence minimizing daily methanol consumption. The last 30 years has seen an increase in aspartame consumption in these areas and with it a significant attenuation of this gradient (91b,95)

An exception to the generalization regarding temperate regions would be expected in areas with established canning industries that are able to offer products so economically as to make the canned product a tempting alternative even in the summer months. For many years both Australia and New Zealand have had such a canning infrastructure and these countries are significant exceptions to the latitude gradient theory. Both have extremely high MS prevalence and incidence numbers (168).

Another exception (albeit in the opposite direction) is Japan which is in the colder latitudes but which has had little MS incidence through most of its recorded history(85,168). Note, however, that the Japanese cultural habit of eating everything in its season did not foster the production or importation of much canned plant material. Although far from tropical, until recently Japan has had one of the lowest rates of methanol consumption per person in the world. This rate has increased with the growing popularity of diet beverages (81,81a). The worlds largest manufacturer of Aspartame is a Japanese company.

Seasonally speaking, in the northern latitudes, before Aspartame, patients with relapsing-remitting MS could expect relapses to be experienced in the winter or Spring (72a) during periods of peak methanol consumption. With increased consumption of diet beverages, Japan and the warmer countries are now reporting their worst relapse period to be the summer (72,72a-b). The difference between warm and cool regions in remission-relapse cycles appears to parallel periods during which toxic canned vegetables and toxic thirst quenchers are most frequently consumed.


Epidemics of MS

There have also been bizarre epidemics or clusters of MS on the Faroe Islands, Orkney and Shetland Islands, and Iceland (84). All of these have been studied in great detail and all involve the influx of massive numbers of British or Allied troops (84,168). One researcher concluded that those individuals most affected were those who had been in direct contact with these troops(168). Another article goes so far as to accuse MS of being a “sexually transmitted infection”(184). An alternative explanation is that these islands had a very low incidence of MS to begin with due the lack of an established canning industry. Troops brought with them items such as canned foods, fruit preserves, marmalades and rations along with the ubiquitous cigarette, all of which would be very desirable to the island people, especially during war time. Methanol consumption was overlooked as a factor in all these studies.


The Scandinavian countries and portions of the Slavic nations have some of the highest incidence of MS of any populations in the world (95a,168). In these countries consumption of canned and home-canned fruits and vegetables is high, as is consumption of smoked-food products and traditional liquors made from rotted culled fruit. Some of these liquors have high enough methanol content to exclude them from international commerce. The alternate name for methanol is “wood alcohol” due to its original source as a condensate product made from wood smoke. Smoked meats and fish are the exception to the rule that animal products do not contain methanol.


The White ManÂ’s Burden

MS was once considered to be a “rich man’s disease” in that its prevalence was positively correlated with the trappings of civilization including modern sanitation practices (85). It now appears that consumption of canned produce provides a better explanation for the relative dearth of MS in many economically depressed regions. To this day the very poorest people of the world are free from autoimmune diseases such as MS (168), lack proper sanitation, and cannot afford canned fruits and vegetables or diet soda.


Identical Symptoms of MS, Methanol Poisoning and Aspartame Toxicity

The symptoms of multiple sclerosis (44,83,85,169), chronic and acute methanol poisoning (13,144,189), and Aspartame toxicity (54,58,93,181), are in all ways identical. There is nothing that happens to the human body from the toxic effect of methanol that has not been expressed during the course of MS…nothing (143,144). This generalization extends even to the remarkable opthomological conditions common to both: transitory optic neuritis and retrolaminar demyelinating optic neuropathy with scotoma of the central visual field (which occasionally manifests as unilateral temporary blindness (85,138,163). In fact, these opthomological symptoms have been thought of for years in their respective literatures to be “tell tale” indications for the differential diagnosis for each of these maladies independently(85,138,148,163,169). The common symptoms of headache(13,83,181,189), nervousness(13,83,181), depression (58,83,189,181), memory loss (18,147,85,169,181), tingling sensations (13,85,168,138,169), pain in the extremities (13,85,169), optic neuritis (85,138,148,163,169), bright lights in the visual field (139,83),seizures (21,83,160) inability to urinate or to keep from urinating (139,146,167) are all shared by each of these conditions and shared yet again by complaints from aspartame poisoning (54,58,93,181). I take these strikingly similar symptom patterns as evidence that these disorders act on identical components of the central nervous system and in the same way.


The “Miracle” that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of methanol has been administered, complete recovery is a possibility. The only two afflictions for which such dramatic “remissions” are reported from identical neuromuscular and opthomological damage, even “blindness” is relapsing-remitting multiple sclerosis (85) and methyl alcohol poisoning (138,163). The pathology of the two maladies is in may ways identical, particularly when it comes to destruction of the myelin sheath with no harm to the axon itself (18,148,176)


Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus (SLE)(73) with fully three-fold representations in infliction numbers over men for both diseases. This is exactly the proportion represented by adverse reactors to Aspartame reported by the US Center for Disease Control in their study of 1984(58). The Center found three women to every man whose Aspartame consumption complaints were serious enough to warrant investigation (93). Although the female/male ratio for those stricken with MS has always been high recent estimates place it at over 3 to 1(91,91a,91c). What might account for the difference across sexes in incidence? A study published in the New England Journal of Medicine (94) reports biopsies of the gastric lining of men and women. A result was that the concentration of ADH in the gastric lining of men was much higher than for woman. Men have the advantage of removing methanol from the bloodstream four times faster on an equal-body-size basis than women. Thus, for men, methanol is more likely to be removed from the blood before it reaches the brain. The brain is spared but the methanol removed would still be metabolized to formaldehyde in the gut where it would reap its havoc on a more forgiving organ. This may help explain why men have more gastrointestinal complaints from both methanol and Aspartame consumption (93,99). On the other hand, womenÂ’s complaints from both more frequently involve serious neurological complications.


MS Cures and treatments

There are no known cures for MS and after reading about all of the many, many treatments, I conclude that the only one that shows statistically valid improvement in double-blind studies, albeit for a relatively short period of time, is plasmapheresis (186). Plasmapheresis involves removing the liquid portion (plasma) of a patientÂ’s blood, then returning the red and white blood cells to the patient without the plasma. Although not done for this reason, the process would be expected to remove much of the methanol from the bloodstream reducing its concentration substantially in the tissues. Transfusions (43) seem also to have similar effect. Viewing methanol toxicity as the ethnologic cause of MS seems to answer all of the nagging question and unexplained anomalies that have stalled the cure for this increasingly persistent disease.



Consumption of aspartame always results in methanol consumption (14,48,51). Methanol will always convert to formaldehyde where it finds an idle ADH (30). When this happens in the brain any protein changed by the formaldehyde will be destroyed by white blood cells (20,23,24,25). The protein most likely destroyed would be myelin basic protein MBP found in the axons. Over a long enough period of time, even without concomitant antibody production, there are those who would call this MS(44). This ends my case for considering methanol to be the cause for multiple sclerosis. Call all this hypothesis and circumstantial evidence if you like. The best experiment to confirm it would never have been allowed by any human subjects committee even though it has been going on for 27 years; and as far as I am concerned it is time to call the experiment complete and to count the bodies. Woodrow C. Monte Ph.D. Professor of Food Science (retired) Page, Arizona Note 1: It has been over 25 years since I heard my first unsolicited plea for help from an Aspartame consumer who had linked consumption of the product to her suffering. My first thought after an hourÂ’s listening was that this courageous young woman would soon be diagnosed with Multiple Sclerosis. It is in her honor that I seek to explain the compelling link between Aspartame, methanol and autoimmunity. Note 2: A fully referenced version of this article will be available at



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